Frequency Therapeutics — Hearing Loss Regeneration

Hope remains for us human beings.

There are many questions and warnings. For example, it is known that if the outer hair cells of the ear die, this is displayed on the audiogram as a loss of the sound sensing thresholds by about 50 dB.
Many here have much less damage, for example, at 14 kHz, the decrease in the perception of the sound senses by 25 -30 dB. This means that the external hair cells themselves are alive, but they are damaged and can not function adequately.

Can technology from "Frequency Therapeutics" help in such cases? Not growing new outer hair cells, but repair, bring the damaged cells to perfect condition?!

In addition, some kind of partial regeneration is possible. But is it 100% complete? Perhaps "Frequency" will be able to return some acceptable thresholds in severe cases, but whether they can return the original ideal hearing is a question mark. Only then will the tinnitus completely disappear. Any loss of sound perception, even by 15 -20 dB, will force the brain to give these spontaneous impulses.

In addition, to be honest, it is unclear how the substance, when introduced into the middle ear, will penetrate into the inner ear, or rather into the cochlea. The cochlea is not a muscle or nervous tissue through which substances can easily penetrate. The cochlea is bone tissue.

As far as I understand, the experiments were carried out only in vitro. But will these results be the same when tested in vivo, that is, in the living body of a person?

Indeed, it is very unlucky that the ear is protected by such a thick bone system.
You ask very good questions, but at the same time your questions remind us that this could be a failing process.

So, please stop analyzing and let the tests show some results.

Then, we can talk a lot about it.

Kind regards
 
Can technology from "Frequency Therapeutics" help in such cases? Not growing new outer hair cells, but repair, bring the damaged cells to perfect condition?!

You need to read up more on Frequency's work., some of your questions have already been answered.

This treatment does not repair the damaged cells, it grows new ones through the activation of Lgr5 progenitor cells.

Also, the stage 1 trial confirmed that the drug cocktail diffuses across the round window membrane via intratympanic injection so your concerns about it penetrating into the inner ear are obsolete.
 
Does the drug take the progenitor cells you have in the your cochlea and multiply them, thereby increasing the chance of fully restored hearing?

The purpose of progenitor cells is to heal any damage. It's how it works in many animals that do have the ability to restore hearing. But for some reason the genes that would allow this process to happen are switched off in mammals after birth. The genes are there and the cells are capable of performing this but the genes are in "off mode" so to say. The hypothesis of the approach using gene therapy is to switch them on and the other approach is to temporarily interfere with the molecule that is keeping the genes switched off which would allow the cells to repair damage without permanently altering the genes in the cells.
 
err...I don't understand what you just said. The drug multiplies the progenitor cells in your cochlea and then makes them into new hairs for hearing. Is that right or wrong?
 
The purpose of progenitor cells is to heal any damage. It's how it works in many animals that do have the ability to restore hearing. But for some reason the genes that would allow this process to happen are switched off in mammals after birth. The genes are there and the cells are capable of performing this but the genes are in "off mode" so to say. The hypothesis of the approach using gene therapy is to switch them on and the other approach is to temporarily interfere with the molecule that is keeping the genes switched off which would allow the cells to repair damage without permanently altering the genes in the cells.
Wow. That would be awesome. Could you provide some type of source that this is the mechanism?
Also- are you saying that this is the mechanism for FX-322?
 
err...I don't understand what you just said.

All of our cells contain all of our DNA (except red blood cells). However all cells don't use all of the genes. In liver cells a set of genes are switched off, in intestine cells a different set of genes are switched off and so on.

Progenitor cells in the inner ear are originally meant to repair any damage in the inner ear. In birds and zebra fish for example, the progenitor cells heal damage in the cochlea.

Humans also have the same type of progenitor cells but our cells don't respond to damage because the genes that should be activated in such response are inhibited by a molecule. So the cells just don't do anything. They just stand there like fools (if you know what I mean).

If we were to activate the genes they should start replacing damaged hair cells.
 
Last edited:
Wow. That would be awesome. Could you provide some type of source that this is the mechanism?
Also- are you saying that this is the mechanism for FX-322?

Try using Google or searching the TT-forums. There's plenty of material. Here's what I found with a simple search:

Cell cycle reactivation of cochlear progenitor cells in neonatal FUCCI mice by a GSK3 small molecule inhibitor.
https://www.ncbi.nlm.nih.gov/pubmed/26643939

Distinct capacity for differentiation to inner ear cell types by progenitor cells of the cochlea and vestibular organs
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5201044/
 
Fx322 better restore hearing and eliminate tinnitus at the same time with the possibility of help hyperacusis and other inner ear disorders.
They better accelerate the process. Any one in here its involved with the trial?


Cure all of us!!!!!!!!
Cure us!!!!!
God Please, let this be a cure.
 
The drug multiplies the progenitor cells in your cochlea and then makes them into new hairs for hearing. Is that right or wrong?

I think it's essentially correct but maybe Silvio can check my understanding.

The drug signals the supporting cells to activate. When they activate, they divide into new cells. Some of these new cells will be more supporting cells, some will be hair cells. The simplicity of this approach is that this a natural process that is temporarily re-activated. The new hair cells are created in the right spot, facing the right way because what is happening is essentially what happens as we develop in our mother's womb and stops happening shortly after we are born.
 
In my understanding this is how it should work according to published information.

They claim cells proliferate, divide and differentiate creating new supporting cells and hair cells colonies maintaining closely the correct pattern and location - "native morphology" , while not overgrowing the cochlear tissue too much or sometimes at all. Tested in vivo and in vitro.
 
is this possible? isn't the trial underway already?
I've talked to the ENT more than a few times now and no the trail is not completely filled. Good news though, I have been pushed on to the the second stage of recruitment. The doctor approved my level of hearing loss for the trial and now I have to be screened by the clinic that is holding the study. My medical history is great and I will get into the study. My blood work have been normal as long as I can remember. I'm getting into the study. Here's to hoping I can pay to get down there and that I'm one of the people who gets the study drug.
 
I've talked to the ENT more than a few times now and no the trail is not completely filled. Good news though, I have been pushed on to the the second stage of recruitment. The doctor approved my level of hearing loss for the trial and now I have to be screened by the clinic that is holding the study. My medical history is great and I will get into the study. My blood work have been normal as long as I can remember. I'm getting into the study. Here's to hoping I can pay to get down there and that I'm one of the people who gets the study drug.
Thank you for your willingness to use your body to potentially help us.
 
I am confused by the fact that in the protocol of the second phase of the FX-322 test, only two reasons are indicated as a criterion for including a patient in the study - by itself, noise-induced hearing loss, and sudden hearing loss (as I understand, idiopathic).

It is a big question why other causes are not included, for example, hearing damage due to ototoxicity of aminoglycosides and so on.

After all, the type of damage between ototoxicity and noise-induced hearing loss are very identical. This is the death of external hair cells as a result of POS and excitotoxicity.

In the exclusion criteria, the presence of a significant autoimmune disease is indicated. That is, this technology is hypothetically not designed for people who have autoimmune hearing loss.

However, I have repeatedly tried to ask these questions from many members of the research group, and I have never received a clear answer.
 
Kind of scared of cancer or an abnormal growth a little bit. Maybe someone who understands the science a little better can ease my mind.
They already had a phase 1 safety study and I would at least think that if those subjects started growing cancers that they would have halted any further testing. Also I think that since it is a direct injection locally to your ear that the dose is also very low.
 
Kind of scared of cancer or an abnormal growth a little bit. Maybe someone who understands the science a little better can ease my mind.

There should be very low risk of this because the theory is that once the drug molecules are cleared from your body through your blood stream, the growth of the cochlear hair cells will stop and return to the previous state of non growth again.

You mention that your tinnitus may be due to skull fracture, if the damage exists past your auditory pathway and is somewhere within your brain center, this may not be fixable via this method. One way to find out if you have actually damage to your cochlear hair cells is get a distortion product otoacoustic emission examine. If this test comes back as showing damage then the Frequency's method will most likely help you.
 
I am confused by the fact that in the protocol of the second phase of the FX-322 test, only two reasons are indicated as a criterion for including a patient in the study - by itself, noise-induced hearing loss, and sudden hearing loss (as I understand, idiopathic).

It is a big question why other causes are not included, for example, hearing damage due to ototoxicity of aminoglycosides and so on.

After all, the type of damage between ototoxicity and noise-induced hearing loss are very identical. This is the death of external hair cells as a result of POS and excitotoxicity.

In the exclusion criteria, the presence of a significant autoimmune disease is indicated. That is, this technology is hypothetically not designed for people who have autoimmune hearing loss.

However, I have repeatedly tried to ask these questions from many members of the research group, and I have never received a clear answer.

Perhaps because they haven't tried it in animal models. When you conduct experiments you have to confine your experiment. You can't test all possibilities at once. It would be unwise of them if they were to include subjects for who's type of hearing loss they have no data from animal testing. It would have been really stupid to have your drug potentially fail not because it's not working but because you made stupid decisions in your trials.

I think people need to stop obsessing about things like: "Why haven't they included this sub-group of tinnitus/hearing loss subjects?".

We currently have 0 drugs or treatments for either tinnitus or hearing loss. Let's get one out on the market. Then when it's out we can always get it prescribed off label.

So first, get that first drug out, then we can start whining about sub-categories.
 
They already had a phase 1 safety study and I would at least think that if those subjects started growing cancers that they would have halted any further testing. Also I think that since it is a direct injection locally to your ear that the dose is also very low.

But what about 10 or 20 or 30 years down the line?
 
After all, the type of damage between ototoxicity and noise-induced hearing loss are very identical. This is the death of external hair cells as a result of POS and excitotoxicity.

Do you have a source for that statement? It's something I've always wondered, especially because my cochlea has been destroyed by otosclerosis, but I don't know exactly what has been broken, and whether it is similar to someone with NIHL or ototoxicity.
 

Log in or register to get the full forum benefits!

Register

Register on Tinnitus Talk for free!

Register Now